Chickenpox is caused by varicella-zoster virus (VZV), a member of the herpesvirus group. The disease occurs in persons with no prior VZV immunity. VZV-specific antibodies can be demonstrated shortly after onset of disease, decline during convalescence, but remain detectable for many years and correlate with immunity to the disease. Chickenpox is highly contagious; over 90% of the population becomes exposed to VZV before they are 20 years old. In most, if not all, cases, VZV apparently becomes latent in dorsal root ganglion cells. From this latent state, VZV can reactivate and cause zoster even in the presence of specific antibodies, probably as a result of weakened cellular immunity. The disease is highly morbid to the immunosuppressed and to those beyond the second decade.
VZV has five major glycoproteins on its surface: gp115 [115 kilodalton (kD) glycoprotein], gp105, gp92, gp83, gp55. These glycoproteins apparently are the products of three genes: gpIII (gp105), gpII (gp115, in the nonreduced state, composed of the reduced species gp62 and gp57), and gpI (gp92, gp83, gp55). Formerly, these genes were referred to as gA, gB, and gC, respectively. Monoclonal (McAb) and polyclonal monospecific antibodies to gA and gB display complement-independent neutralization, and such antibodies to gC display complement-dependent neutralization of VZV.